Kymera Therapeutics to Share Novel Preclinical Findings Reinforcing the Advantage of IRAK4 Degraders over Kinase Inhibitors as well as First STAT3 Degrader Results in a Preclinical Model of Th17 Inflammation
-Data to be shared at the American Association of Immunologists (AAI) Annual Meeting
-Results highlight potential for IRAK4 degraders to broadly impact TLR/IL-1R-driven inflammatory and autoimmune diseases in a manner superior to kinase inhibitors
-Findings support further exploration of STAT3 degraders in Th17-driven autoimmune indications
Excerpt from the Press Release:
WATERTOWN, Mass., May 05, 2022 (GLOBE NEWSWIRE) — Kymera Therapeutics, Inc. (NASDAQ: KYMR), a clinical-stage biopharmaceutical company advancing targeted protein degradation to deliver novel small molecule protein degrader medicines, today presented new preclinical results demonstrating that STAT3 degradation alleviates Th17 inflammation and is active in a preclinical animal model of CNS inflammation, and that IRAK4 degradation blocks multiple innate immune signaling pathways across different immune cell types in a manner superior to kinase inhibitors. Data will be shared in two separate posters at the American Association of Immunologists (AAI) Annual Meeting 2022, taking place from May 6 – 10, 2022 in Portland, Oregon.
“Collectively, the findings demonstrate the advantage of using degraders to effectively drug signaling nodes driving inflammation as well as the translation of in vitro activity to in vivo proof of concept in animal models of autoimmune disease,” said Anthony Slavin, Vice President, Immunology. “The impact of STAT3 degradation on immune and stromal cell activation and Th17 inflammation leading to potent effects in a mouse model of multiple sclerosis, as well as the broad effect of IRAK4 degradation on TLR-mediated signaling and cytokine induction and its superiority to kinase inhibition, underscore the clinical potential of these degraders in the treatment of inflammatory and autoimmune disorders.”
STAT3 is a transcriptional regulator that has been linked to numerous cancers as well as multiple autoimmune and fibrotic diseases. Heterobifunctional degraders have emerged as a novel therapeutic modality with great potential to drug historically “undruggable” protein targets like STAT3. Kymera has previously shown its selective STAT3 degraders can suppress the growth of tumors in preclinical models of lymphoma and solid tumors. Findings presented at AAI reveal for the first time the activity of Kymera’s STAT3 degraders against Th17 inflammation, including in vivo proof of concept in a clinically relevant mouse experimental autoimmune encephalitis (EAE) model of multiple sclerosis. Degradation of STAT3 inhibited Th17 development and cytokine release, which in turn blocked disease induction and also mitigated ongoing disease in the EAE model.
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